<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE235nnn/GSE235686/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE235686</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Acute Myeloid Leukemia patient/ CD34+ healthy donor RNA-seq</name><description>AML is an aggressive and heterogenous hematologic malignancy. Here, we performed bulk RNA sequencing of 16 AML patients and primary hematopoietic cell populations, CD34+ HSC and CD14+monocytes to understand transcriptional and post-transcriptional mechanisms that drive leukemogenesis and block AML differentiation. Our findings provide a better understanding of gene regulatory pathways in AML in comparison to normal hematopoietic cells, which may provide new therapeutic strategy to selectively target AML cells.</description><dates><publication>2026/06/01</publication></dates><accession>GSE235686</accession><cross_references><GSM>GSM7507895</GSM><GSM>GSM7507896</GSM><GSM>GSM7507893</GSM><GSM>GSM7507894</GSM><GSM>GSM7507891</GSM><GSM>GSM7507892</GSM><GSM>GSM7507890</GSM><GSM>GSM7507903</GSM><GSM>GSM7507904</GSM><GSM>GSM7507901</GSM><GSM>GSM7507902</GSM><GSM>GSM7507899</GSM><GSM>GSM7507888</GSM><GSM>GSM7507900</GSM><GSM>GSM7507889</GSM><GSM>GSM7507897</GSM><GSM>GSM7507898</GSM><GPL>24676</GPL><GSE>235686</GSE><taxon>Homo sapiens</taxon></cross_references></HashMap>